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  • 1
    Keywords: Medicine ; Pharmacology ; Biomedicine ; Pharmacology/Toxicology ; Springer eBooks
    Description / Table of Contents: G Protein-Coupled Receptor Kinases (GRKs) History: Evolution and Discovery -- Structure and Function of G Protein-Coupled Receptor Kinases 1 and 7 -- Visual G Protein-Coupled Receptor Kinases -- Molecular Basis for Targeting, Inhibition, and Receptor Phosphorylation in the G Protein-Coupled Receptor Kinase 4 Subfamily -- “Barcode” and Differential Effects of GPCR Phosphorylation by Different GRKs -- Cell-Type Specific GRK2 Interactomes: Physiopathological Implications -- Differential Regulation of IGF-1 and Insulin Signaling by GRKs -- Differential Control of Potassium Channel Activity by GRK2 -- Critical Role of GRK2 in the Prevention of Chronic Pain -- Roles of GRK Dysfunction in Alzheimer’s Pathogenesis -- Regulation of Dopamine-Dependent Behaviors by G Protein-Coupled Receptor Kinases -- G Protein-Coupled Receptors and Their Kinases in Cardiac Regulation -- GRK Roles in C. elegans -- Evolutionarily Conserved Role of G Protein-Coupled Receptor Kinases in the Hedgehog Signaling Pathway
    Abstract: This collection explores up-to-date descriptions of known G protein-coupled receptor kinase (GRK)-dependent mechanisms, both associated with G protein-coupled receptor (GPCR) functions and the receptor-independent. The chapters cover a wide range of studies from invertebrates to humans, with sections of the volume covering GRK structure, mechanisms of activation, and interaction with GPCRs, GRKs in cell signaling, as well as physiological and pathophysiological mechanisms regulated by GRKs. Written for the Methods in Pharmacology and Toxicology series, this book features the kind of practical detail necessary for success in the laboratory. Authoritative and timely, G Protein-Coupled Receptor Kinases features the kind of comprehensive mechanistic elucidation of GRK functions and their regulation in cells necessary for a better understanding of cell biology as well as for devising novel research approaches and therapeutic strategies
    Pages: XI, 329 p. 36 illus., 33 illus. in color. : online resource.
    ISBN: 9781493937981
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  • 2
    Keywords: Medicine ; Gene Therapy ; Toxicology ; Biochemistry ; Cell receptors ; Cytology ; Biomedicine ; Pharmacology/Toxicology ; Biochemistry, general ; Protein Structure ; Gene Therapy ; Cell Physiology ; Receptors ; Springer eBooks
    Description / Table of Contents: Therapeutic Potential of Small Molecules and Engineered Proteins.-Arrestin Interactions with G Protein-coupled Receptors -- Arrestin-biased GPCR℗ Agonists -- Arrestin-1 Expression Levels, Rod Function and Health -- Protective Functions of Arrestin-1 in Photoreceptors -- Arrestin-4 and Cone Function -- Enhanced Phosphorylation-independent Arrestins and Gene Therapy -- Targeting Particular Receptors with Redesigned Non-visual Arrestins.-℗ Arrestins binding to clathrin, AP2 and Role in GPCR trafficking -- Arrestins in Ubiquitination and Deubiquitination -- Arrestin Self-association -- Arrestin-dependent Activation of ERK and Src -- Arrestin-dependent Activation of JNK Family Kinases -- Arrestin-Mediated P38 Activation.-℗ Arrestin-dependent PDE Localization -- Arrestins in Cell Migration -- Arrestins in Host-pathogen Interactions -- Arrestin Regulation of Small GTPases -- GPCRs and Arrestins in Airways: Implications for Asthma -- Arrestins as Regulatory Signaling Hubs in Cancer Pathways -- Arrestins in Pain and Anesthesia
    Abstract: This volume describes our current understanding of the biological role of visual and non-visual arrestins in different cells and tissues, focusing on the mechanisms of arrestin-mediated regulation of GPCRs and non-receptor signaling proteins in health and disease. The book covers wide range of arrestin functions, emphasizing therapeutic potential of targeting arrestin interactions with individual partners
    Pages: VIII, 447 p. 53 illus., 42 illus. in color. : online resource.
    ISBN: 9783642411991
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  • 3
    Unknown
    Cham : Springer International Publishing
    Keywords: Life sciences ; Biochemistry ; Proteins ; Life sciences ; Animal Biochemistry ; Protein Science ; Protein Structure ; Springer eBooks
    Description / Table of Contents: Arrestins: discovery of the family and functional role of conformational flexibility -- Overview of arrestin-mediated signaling with receptors and non-receptor binding partners -- Initial crystallographic studies of visual arrestin: insights and perspectives -- Structural basis for b-arrestins in GPCR trafficking -- Arrestin-3: the structural basis of lower receptor selectivity -- Phosphate sensor and construction of phosphorylation-independent arrestins -- Comprehensive analysis of the role of arrestin residues in receptor binding -- How arrestin recognizes and binds active GPCRs -- Localization of conformational dynamics of arrestins by HDX-MS -- GPCR footprint on arrestins and manipulation of receptor specificity -- The structure of the polar core mutant R175E and its functional implications -- Active conformations of arrestins: expected and unexpected changes -- The arrestin-receptor complex: exciting answers and new questions -- Scaffolding c-Jun N-terminal kinase cascades: mechanistic insights from the reconstituted arrestin-JNK cascades -- Arrestin-dependent ERK activation and its disruption -- The functional role of the conformational changes in arrestin upon activation -- Is signaling specificity encoded in arrestin conformation? -- Monofunctional elements of multi-functional arrestin proteins -- Arrestins in cell death
    Abstract: This volume summarizes our current understanding of the structural basis of the functions of arrestin family of proteins. Arrestins were first discovered as key players in the desensitization of G protein-coupled receptors (GPCRs). Recent studies showed that arrestins are important signal transducers in their own right, organizing multi-protein complexes and scaffolding numerous signaling cascades that regulate cell proliferation, differentiation, and apoptotic death. Here arrestin functions are described primarily from the structural prospective. The book covers basal structure of arrestin proteins, receptor binding-induced conformational changes in arrestins, as well as the structure of “pre-activated” mutants. Particular focus is on the arrestin elements interacting with numerous binding partners, GPCRs and cytoplasmic signaling proteins. We expect that this information and insights will help to understand and exploit the phenomenon of signaling bias, which is a new promising direction in drug discovery. The chapters are written by the world-class specialists in the field, mostly the people who actually contributed the data discussed. The book gives coherent historical prospective and describes the most recent findings. The book would be particularly useful for scientists in academia and industry working in the fields of pharmacology, cell biology, structural biology, and drug discovery. We expect that the focus on the molecular basis of protein-protein interactions would help to develop novel tools for engaging this important type of targets for research and therapeutic purposes
    Pages: IX, 304 p. 53 illus., 51 illus. in color. : online resource.
    ISBN: 9783319575537
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  • 4
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Arrestins and G protein-coupled receptor kinases (GRKs) are key players in homologous desensitization of G protein-coupled receptors. Two non-visual arrestins, arrestin2 and 3, and five GRKs (GRK2, 3, 4, 5 and 6) are involved in desensitization of many receptors. Here, we demonstrate a steady increase in arrestin2 expression during prenatal development. The density of arrestin2 mRNA is higher in differentiated areas as compared with proliferative zones, whereas arrestin3 mRNA shows the opposite distribution. At embryonic day 14, concentrations of arrestin proteins are similar (32–34 nm). Later in development, arrestin2 expression rises, leading to a fourfold excess of arrestin2 over arrestin3 at birth (48 vs. 11 ng/mg protein or 102 vs. 25 nm). Among GRKs, only GRK5 increased with embryonic age from 124 nm at E14 to 359 nm at birth. Similarly, in vitro differentiation of cultured precursor cells, neurospheres, leads to a significant up-regulation of arrestin2 resulting in 〉 20-fold excess of arrestin2 (160 vs. 7 nm). GRK5 is the only subtype increased with neurosphere differentiation, although the change is only about twofold. The data demonstrate selective increases in the expression of arrestin2 associated with neural development and suggest specific yet unappreciated roles for arrestin2 in neural differentiation.
    Type of Medium: Electronic Resource
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  • 5
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    The American Association for the Advancement of Science (AAAS)
    Publication Date: 2018-09-26
    Description: Several studies have suggested that arrestin-mediated signaling by GPCRs requires G protein activation; however, in this issue of Science Signaling , Luttrell et al. documented arrestin-dependent activation of ERK1/2 by a number of GPCRs. These studies do not contradict each other, but illustrate the complexity of cellular signaling that cannot and should not be reduced to simplistic models.
    Print ISSN: 1945-0877
    Topics: Medicine
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  • 6
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Solid State Ionics 38 (1990), S. 241-249 
    ISSN: 0167-2738
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 0168-9002
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 0223-5234
    Keywords: 1,4-dihydropyridine ; [abr] ADP; adenosine 5'-diphosphate ; [abr] ATP; adenosine 5'-triphosphate ; [abr] ATPase; adenosine 5'-triphosphatase ; [abr] DCC; N,N'-dicyclohexylcarbodiimide ; [abr] EGTA; ethylene glycolbis(β-aminoethyl ether) ; [abr] NADPH; nicotinamide adenine dinucleotide phosphate, reduced form ; [abr] TBA; thiobarbituric acid ; [abr] TRIS; tris(hydroxymethyl)aminomethane ; antiplatelet agent ; taurine
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 0370-2693
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 0375-9474
    Keywords: Nuclear Reactions
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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